Skeletal muscle and its associated connective tissue comprises approximately 40% of the total human body. With increased age, the average human being looses about 20% of their skeletal muscle mass by the age of 70. Appropriate structure and function of skeletal muscle is required for muscle contraction and relaxation, and the maintenance of body posture. Although much attention has been paid to the crippling effects of bone thinning, muscle loss (sarcopenia) causes unsteadiness in the legs that leads to falls. Sarcopenia reduces mobility, stair climbing, ability to get in and out of chairs, reduces quality of life, and will led aged adults into a more unhealthy sedentary lifestyle. Skeletal muscle satellite cells are responsible for the regeneration of muscle fibers and their activation is regulated, in part, by the extrinsic extracellular environment. The potential for extracellular matrix marcomolecules to influence satellite cell activation is significant. In particular, the proteoglycan component which can both regulate cell proliferation and differentiation, and collagen fibril organization. Both of thee properties will have a significant impact on muscle repair and function. In the proposed experimental strategy, we will use the avian Low Score Normal (LSN) genetic muscle weakness in which alterations in decorin proteoglycan expression, collagen crosslinking, and satellite cell proliferation and differentiation have already been demonstrated. The objectives of the research are to: 1. Characterize proteoglycan and decorin synthesis from control and LSN satellite cells; and 2. To determine the temporal and spatial localization of decorin and type I collagen. The results from this proposed investigation are significant in the development of strategies to alleviate sarcopenia and for furthering the understanding of the extracellular matrix in the activation of satellite cells with muscle aging.